SELECTION

(Prepared by: Isha Gaikwaid, 20220901015)

Viruses undergo evolution and natural selection, just like cell-based life, and most of them evolve rapidly. When two viruses infect a cell at the same time, they may swap genetic material to make new, "mixed" viruses with unique properties. For example, flu strains can arise this way. RNA viruses have high mutation rates that allow especially fast evolution. An example is the evolution of drug resistance in HIV.

Have you ever wondered why a different strain of flu virus comes around every year? Or how HIV, the virus that causes AIDS, can become drug-resistant?

The short answer to these questions is that viruses evolve. That is, the "gene pool" of a virus population can change over time. In some cases, the viruses in a population—such as all the flu viruses in a geographical region, or all the different HIV particles in a patient's body—may evolve by natural selection. Heritable traits that help a virus reproduce (such as high infectivity for influenza, or drug resistance for HIV) will tend to get more and more common in the virus population over time.

Let's see what are types of selection seen in evolution of viruses.

1) HOST IMMUNE SYSTEM: The immune system of the host is constantly trying to eliminate viruses. Therefore, viruses that can evade the host's immune system are more likely to survive and reproduce. Over time, this can lead to the evolution of viruses that are better adapted to their host's immune system.

                                           Source: https://www.frontiersin.org/articles/10.3389/fimmu.2018.00320/full

2) DRUG SELECTION: When viruses are exposed to drugs, those that are resistant to the drug are more likely to survive and reproduce. This can lead to the evolution of drug-resistant viruses.

                   Source: https://www.futuremedicine.com/doi/10.2217/17460794.1.3.361

3) TRANSMISSION SELECTION: Viruses that can spread more easily from host to host are more likely to survive and reproduce. This can lead to the evolution of viruses that are better adapted to transmission between hosts.

                                  Source:https: https://www.sciencedirect.com/science/article/pii/S0195670115003679

4) REPLICATION SELECTION: Viruses that can replicate more quickly are more likely to survive and reproduce. This can lead to the evolution of viruses that are better adapted to replicating quickly within a host. 

                Source: //www.immunology.org/public-information/bitesized-immunology/pathogens-disease/virus-replication

NATURAL SELECTION AND MOLECULAR EVOLUTION IN FUSARIUM GRAMINEARUM 

VIRUS 1

We aimed to investigate the evolution and adaptation of Fusarium graminearum virus 1 (FgV1), a positive-sense ssRNA virus that induces hypovirulence in its fungal host. As FgV1 lacks an extracellular life cycle and is transmitted through sporulation or hyphal anastomosis, we conducted mutation accumulation (MA) experiments by serially passaging FgV1 alone or with FgV2, 3, or 4 in F. graminearum to understand its evolutionary dynamics. We hypothesized that the effects of positive selection on the virus would be constrained due to repeated bottleneck events. 

Determine whether selection on FgV1 was positive, negative, or neutral, we evaluated both the host fungus's phenotypic traits and the RNA sequences of FgV1. Our results indicated that positive selection acted on beneficial mutations in FgV1, as evidenced by the dN/dS ratio, pNR/pNC ratio, and changes in predicted protein structures. Specifically, we observed evidence of positive selection only in the open reading frame 4 (ORF4) protein of DK21/FgV1 (MA line 1), where mutations at amino acids 163A and 289H affected the entire structure of the protein predicted to be under positive selection.

                                   Source: https://www.frontiersin.org/articles/10.3389/fmicb.2021.622261/full

However, our findings also revealed that deleterious mutations played a significant role in FgV1's evolution during serial passages. The relationship between changes in viral fitness and the number of mutations in each MA line showed that some deleterious mutations led to a decline in fitness. Additionally, we observed that some mutations in MA line 1 were unique and not shared with any of the other four MA lines (PH-1/FgV1, PH-1/FgV1 + 2, PH-1/FgV1 + 3, and PH-1/FgV1 + 4), indicating that evolutionary pathways of the virus might differ with respect to hosts and co-infecting viruses. We suggested that mutational robustness and other unidentified factors could also contribute to the observed differences among MA lines. Thus, further research is needed to clarify the effects of virus co-infection on the adaptation or evolution of FgV1 in its environments.

References

https://doi.org/10.3389/fmicb.2020.600775